The effect of mutations in prm, the promoter for repressor maintenance, on the synthesis of the lambda cI repressor and rex proteins, will be studied genetically and biochemically to learn more about regulation of lysogenization by lambda. Specifically, we intend to determine the mechanism by which one mutation, prm116, simultaneously prevents repressor synthesis on infection of a lysogen when prm should be active, but causes overproduction of repressor on infection of a non- lysogen, when pre, a second promoter for cI-rex transcription, should be active. In addition, several new prm mutants are being tested for their effects on repressor synthesis in vivo, to see if all or only some prm mutants cause overproduction. The mutants will also be analyzed for their effects on cro, repressor, and RNA polymerase binding in the lambda prm-OR-PR region. Finally, studies of the role of rex function in the lambda life cycle are being continued although as yet, no role for rex protein has been determined. Bibliographic references: G.N. Gussin, K-M. Yen, and L.F. Reichardt (1975). Repressor synthesis in vivo after infection of E. coli by a prm mutant of bacteriophage lambda. Virology 63: 273-277; G. N. Gussin and K.M. Yen (1975). Effect of a prm mutant on regulation of lambda repressor synthesis. Biol. of Temperate Bacteriophage, 5th Int. Conf., p. 86 (Abst.).